Prinzmetal Angina and Cyproheptadine

Dr. Ambrus emphasizes that inhibition of platelet aggregation is a potential important pathophysiologic mechanism for serotonergic-receptor blockade in vasospasm. Serotonin is initially released when platelets aggregate and initiate a positive feedback loop by releasing adenosine diphosphate, thromboxane A2, and more serotonin.

An early study [1] failed to show a decrease in the number of ischemic episodes in patients with vasospastic angina who were treated with ketanserin, a selective serotonin-receptor (S2) antagonist. Ketanserin was given at concentrations that inhibited in vitro platelet aggregation. The presence of serotonin-receptor families, individual patient characteristics for platelet aggregation, and differing in vivo responses may make the use of other serotonin-receptor antagonists, such as cyproheptadine, clinically efficacious in selected patients.